liver disease

oh, the patient with jaundice. what can I do?

The jaundiced patient must be always taken seriously, and an accurate preoperative diagnosis of the cause is important. Three major category of diseases can cause jaundice:

• prehepatic( unconjugated hyperbilirubinemia)
• hemolytic anemias
• gilbert syndrome
• Crigler Najar syndrome
• hepatic parynchemal diseases, furthur divided into acute or chronic
• biliary obstruction(intrahepatic or extrahepatic)

preoperative considerations:
an accurate daignosis of the type and cause of jaundice can be reached by taking a careful history, a review of liver function tests, and other investigations.
history:
history of family jaundice, contact with jaundice patient, blood transfusion, tattooing, acupuncture, drug addiction,foreign travel, alcoho; intake, general health, and occupational hazards.
investigations:
liver function tests
full blood count:
A low blood count may be the result of concealed blood loss or hemolysis.
A raised white blood count may be seen with cholicystitis or cholangitis.
urea and electrolytes:
rising urea is important and require uergent treatment.
clotting studies:
PT may be prolonged.
virology:
hepatitis B may need to be excluded.
radiograpgs:
chest; both cholecystitis and hepatomegaly inhibit right sided diaphragmatic movements, thus giving a propensity for lower right chest infections and pulmonary effusions.
abdominal; only in aminority of cases the radiograph shows gall stones (ground glass appearance).
barium meal or endoscopy: it will reveal esophageal varices. distorsion and fixation od doudenum occurs in carcinoma of pancreas.
cholangiography: ERCP has a low complication rate and is effective at demonstrating the site of obstruction,even when the obstruction is complete.
ultrasonography and CT
thes investigations will demonstrate grossly dilated ducts and will give information about liver parynchema, gall baldder, and even the site of obstruction.
liver biopsy:
percutaneous needle biopsy is now accepted as a routine investigation in liver diseases.
the perioperative management  depends on reaching a correct diagnosis of the type and cause of jaundice.

anesthesia for hepatobilliary diseases ppt presentation

Anesthesia for liver cirrhosis

CIRRHOSIS



Cirrhosis is a serious and progressive disease that eventually results in hepatic failure.

causes include

• chronic active hepatitis (postnecrotic cirrhosis),
• chronic biliary inflammation or obstruction (primary biliary cirrhosis, sclerosing cholangitis),
• chronic right-sided congestive heart failure (cardiac cirrhosis),
• autoimmune hepatitis,
• hemochromatosis,
• Wilson's disease,
• 1-antitrypsin deficiency,
• nonalcoholic steatohepatitis, and
• cryptogenic cirrhosis.

Preoperative Considerations


Patients with cirrhosis are at increased risk for deterioration of liver function because of their limited functional reserves.
Successful anesthetic management of these patients is dependent on recognizing the multisystem nature of cirrhosis and controlling or preventing its complications

Gastrointestinal Manifestations

Portal hypertension (> 10 mm Hg) leads to the development of extensive portal-systemic venous collateral channels. Four major collateral sites are generally recognized: gastroesophageal, hemorrhoidal, periumbilical, and retroperitoneal.
In patients with cirrhosis, massive bleeding from gastroesophageal varices is a major cause of morbidity and mortality. In addition to the effects of acute blood loss, the increased nitrogen load (from the breakdown of blood in the intestinal tract) can precipitate hepatic encephalopathy.
The treatment of variceal bleeding is generally supportive (medical).
Blood loss should be replaced with intravenous fluids and blood products.
Nonsurgical treatment includes vasopressin (0.1–0.9 U/min intravenously), somatostatin (250 g followed by 250 g/h), propranolol, balloon tamponade (with a Sengstaken–Blakemore tube), and endoscopic sclerosis of the varices.
Percutaneous transjugular intrahepatic portosystemic shunts (TIPS) can reduce portal hypertension and subsequent bleeding (however, it may increase the incidence of encephalopathy).
When the bleeding fails to stop or it recurs, emergency surgery may be indicated. Surgical risk has been shown to correlate with the degree of hepatic impairment, based on clinical and laboratory findings. Shunting procedures are generally performed on low-risk patients, whereas ablative surgery, esophageal transection, and gastric devascularization are reserved for high-risk patients.

Child's Classification for Evaluating Hepatic Reserve.1
Risk Group                            A                                         B                                           C
Bilirubin (mg/dL)                 < 2.0                              2.0–3.0                                       > 3.0
Serum albumin (g/dL)           > 3.5                            3.0–3.5                                        < 3.0
Ascites                                None                           Controlled                               Poorly controlled
Encephalopathy                  Absent                          Minimal                                   Coma
Nutrition                             Excellent                        Good                                      Poor
Mortality rate (%)                 2–5                              10                                                    50


Hematological Manifestations

Anemia, thrombocytopenia, and, less commonly, leukopenia, may be present. The cause of the anemia is usually multifactorial and includes blood loss, increased red cell destruction, bone marrow suppression, and nutritional deficiencies.
Congestive splenomegaly (from portal hypertension) is largely responsible for the thrombocytopenia and leukopenia.
Coagulation factor deficiencies arise as a result of decreased hepatic synthesis. Enhanced fibrinolysis secondary to decreased clearance of activators of the fibrinolytic system may also contribute to the coagulopathy.
coagulopathy should be corrected before surgery. Clotting factors should be replaced with appropriate blood products such as FFP and cryoprecipitate.
Platelet transfusions should be considered immediately prior to surgery for counts less than 100,000/ L.

what you should remember about liver

HEPATIC PHYSIOLOGY & ANESTHESIA :


FUNCTIONAL ANATOMY
The liver is separated by the falciform ligament into right and left anatomic lobes; the larger right lobe has two additional smaller lobes at its posterior–inferior surface, the caudate and quadrate lobes. In contrast, surgical anatomy divides the liver based on its blood supply. Thus the right and left surgical lobes are defined by the point of bifurcation of the hepatic artery and portal vein (porta hepatis); the falciform ligament therefore divides the left surgical lobe into medial and lateral segments. Surgical anatomy defines a total of eight segments.
The liver is made up of 50,000–100,000 discrete anatomic units called lobules. Each lobule is composed of plates of hepatocytes arranged cylindrically around a centrilobular vein. Four to five portal tracts, composed of hepatic arterioles, portal venules, bile canaliculi, lymphatics, and nerves, surround each lobule.

In contrast to a lobule, an acinus, the functional unit of the liver, is defined by a portal tract in the middle and centrilobular veins at the periphery. Cells closest to the portal tract (zone 1) are well oxygenated; those closest to centrilobular veins (zone 3) receive the least oxygen and are most susceptible to injury.